Bursicon, a Neuropeptide Hormone That Controls Cuticle Tanning and Beyond

Abstract

Insects are encased in a semi-rigid exoskeleton, which provides protection, locomotion, and internal attachments sites for muscles and internal organs. However, it also limits insect's growth. Insect must shed its old exoskeleton periodically (molting) in order to grow. After each molt, the newly formed exoskeleton is usually soft, lightly pigmented and flexible, permitting insect to extend its body size for growth.Sclerotization of newly formed cuticle must occur in a relatively short period of time after each molt and completion of body expansion in order for the new exoskeleton to be functional for protection. Insects could not survive without properly hardened cuticle. Molting and cuticle sclerotization in insects are regulated by a precise coordination of at least 6 hormones including prothoracicotropic hormone (PTTH), 20-hydroxyecdysone (20E), eclosion hormone (EH), ecdysis triggering hormone (ETH), crustacean cardioactive peptide (CCAP) and bursicon. In our previous chapter (Song and Sun 2005 edited by Liu and Kang), we already introduced signal transduction pathways of PTTH, 20E and JH. Here in this chapter, we would like to summarize the molecular mechanisms of EH, ETH, CCAP and bursicon and their coordination in regulating the final steps of the molting process i.e. ecdysis and cuticle sclerotization. In particular, we will focus on the action of bursicon. The elucidation of the key biochemical events leading to cuticle sclerotization would add an important body of knowledge towards understanding insect development and for designing more efficient pest control strategies to disrupt the cuticle sclerotization process.